Evidence map›Paper›PMID 20623734›Full record

ArticleEMBO molecular medicine2010

Oncolytic targeting of renal cell carcinoma via encephalomyocarditis virus.

Frederik C Roos, Andrew M Roberts, Irene I L Hwang, Eduardo H Moriyama, Andrew J Evans, Stephanie Sybingco, Ian R Watson, Leticia A M Carneiro, Craig Gedye, Stephen E Girardin and 7 more

Open access · goldAbstract read
In one paragraph

Article in EMBO molecular medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Review
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  7. Review
  8. Article
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  11. Article
  12. Article
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  14. The oncolytic activity of Newcastle disease virus in clear cell renal carcinoma cells in normoxic and hypoxic conditions: the interplay between von Hippel-Lindau and interferon-β signaling.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2013
    Article
  15. Interferon-γ-induced necrosis: an antitumor biotherapeutic perspective.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2013
    Review
  16. Article
  17. Oncolytic virotherapy.Nature biotechnology · 2012
    Review
  18. Review
  19. Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

17 authors at 5 institutions in 2 countries.

Frederik C RoosDepartment of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada.
Andrew M Roberts
Irene I L Hwang
Eduardo H Moriyama
Andrew J Evans
Stephanie Sybingco
Ian R Watson
Leticia A M Carneiro
Craig Gedye
Stephen E Girardin
Laurie E Ailles
Michael A S Jewett
Michael Milosevic
Brian C Wilson
John C Bell
Sandy D Der
Michael Ohh
University of Toronto · CAOntario Institute for Cancer Research · CAPrincess Margaret Cancer Centre · CAUniversity Health Network · CAJohannes Gutenberg University Mainz · DE

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

Apoptosis is a fundamental host defence mechanism against invading microbes. Inactivation of NF-kappaB attenuates encephalomyocarditis virus (EMCV) virulence by triggering rapid apoptosis of infected cells, thereby pre-emptively limiting viral replication. Recent evidence has shown that hypoxia-inducible factor (HIF) increases NF-kappaB-mediated anti-apoptotic response in clear-cell renal cell carcinoma (CCRCC) that commonly exhibit hyperactivation of HIF due to the loss of its principal negative regulator, von Hippel-Lindau (VHL) tumour suppressor protein. Here, we show that EMCV challenge induces a strong NF-kappaB-dependent gene expression profile concomitant with a lack of interferon-mediated anti-viral response in VHL-null CCRCC, and that multiple established CCRCC cell lines, as well as early-passage primary CCRCC cultured cells, are acutely susceptible to EMCV replication and virulence. Functional restoration of VHL or molecular suppression of HIF or NF-kappaB dramatically reverses CCRCC cellular susceptibility to EMCV-induced killing. Notably, intratumoural EMCV treatment of CCRCC in a murine xenograft model rapidly regresses tumour growth. These findings provide compelling pre-clinical evidence for the usage of EMCV in the treatment of CCRCC and potentially other tumours with elevated HIF/NF-kappaB-survival signature.

Indexed as

AnimalsApoptosisBasic Helix-Loop-Helix ProteinsCarcinoma, Renal CellCell Line, TumorEncephalomyocarditis virusEndothelial PAS Domain-Containing Protein 1Kidney NeoplasmsMiceMice, SCIDNF-kappa BOncolytic VirusesRNA InterferenceRNA, Small InterferingSignal TransductionTransplantation, HeterologousBasic Helix-Loop-Helix ProteinsEndothelial PAS Domain-Containing Protein 1NF-kappa BRNA, Small InterferingVon Hippel-Lindau Tumor Suppressor Protein

Identifiers

PMID20623734
PMCPMC3377327
OpenAlexW2132181817

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.